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Cyclosporin suppresses transplant arteriosclerosis in the aorta-allografted, cholesterol-clamped rabbit. Suppression

H O Andersen1, G Madsen, B G Nordestgaard

  • 1Department of Clinical Biochemistry, Rigshospitalet, Copenhagen O, Denmark.

Arteriosclerosis and Thrombosis : a Journal of Vascular Biology
|June 1, 1994
PubMed

Insights

Cyclosporin significantly reduces transplant arteriosclerosis in rabbits by inhibiting myointimal proliferation and decreasing aortic permeability to low-density lipoprotein. This immunosuppressant offers a potential therapeutic benefit for heart transplant recipients.

Area of Science:

  • Cardiovascular Research
  • Transplantation Immunology
  • Pharmacology

Background:

  • Transplant arteriosclerosis is a major long-term complication following heart transplantation.
  • The role of the immunosuppressant cyclosporin in transplant arteriosclerosis is controversial, with suggestions of both aggravation and retardation.
  • Understanding cyclosporin's precise effect is crucial for managing heart transplant outcomes.

Purpose of the Study:

  • To investigate the effect of human therapeutic levels of cyclosporin on experimental transplant arteriosclerosis.
  • To determine if cyclosporin influences the development of arteriosclerosis in aortic transplants.
  • To elucidate the mechanisms underlying cyclosporin's impact on transplant arteriosclerosis.

Main Methods:

  • A rabbit model of aortic transplantation was utilized.
  • Plasma cholesterol levels were maintained at 5-7 mmol/L in hyperlipidemic groups.
  • Cyclosporin was administered at human therapeutic levels.
  • Biochemical and histological assessments quantified transplant arteriosclerosis severity.
  • Low-density lipoprotein permeability in transplanted aortas was measured.

Main Results:

  • Cyclosporin markedly suppressed transplant arteriosclerosis severity.
  • Cholesterol content in aortic transplants was reduced by 70% (10 days) and 80% (20 days) in cyclosporin-treated rabbits (P < .01).
  • Myointimal proliferation was completely inhibited after 20 days of cholesterol feeding in cyclosporin-treated animals (P < .05).
  • Cyclosporin reduced aortic permeability to low-density lipoprotein by 90% (P < .01) in non-cholesterol-fed rabbits.

Conclusions:

  • Cyclosporin significantly decreases the severity of transplant arteriosclerosis.
  • The protective effect of cyclosporin appears to be mediated, in part, by reducing aortic lipoprotein permeability.
  • These findings suggest a beneficial role for cyclosporin in preventing transplant arteriosclerosis in heart transplant patients.

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